Novel Uncoupling Proteins

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. Charles Affourtit,
  2. Paul G. Crichton,
  3. Nadeene Parker and
  4. Martin D. Brand

Published Online: 20 MAY 2008

DOI: 10.1002/9780470725207.ch6

Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287

Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287

How to Cite

Affourtit, C., Crichton, P. G., Parker, N. and Brand, M. D. (2007) Novel Uncoupling Proteins, in Mitochondrial Biology: New Perspectives: Novartis Foundation Symposium 287 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470725207.ch6

Author Information

  1. MRC Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 2XY, UK

  1. This paper was presented at the symposium by Martin Brand, to whom correspondence should be addressed.

Publication History

  1. Published Online: 20 MAY 2008
  2. Published Print: 5 OCT 2007

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470066577

Online ISBN: 9780470725207

SEARCH

Keywords:

  • mitochondrial proton leak;
  • uncoupling proteins;
  • mild uncoupling;
  • reactive oxygen species;
  • oxidative damage;
  • degenerative disease;
  • ageing;
  • pancreatic beta cells;
  • insulin secretion

Summary

Mitochondria are incompletely coupled because of proton leaks that shortcircuit oxidative phosphorylation. Basal proton leak is unregulated and is associated with the presence (but not catalytic activity) of the adenine nucleotide translocase. Inducible proton leak is regulated and is catalysed by the adenine nucleotide translocase and specific uncoupling proteins (UCPs). UCP1 catalyses proton conductance in mammalian brown adipose tissue. It is activated by fatty acids, which overcome nucleotide inhibition. UCP2, UCP3 and UCPs from birds, fish and plants also catalyse proton conductance that is inhibited by nucleotides. However, they require activation by superoxide or other reactive oxygen species (ROS). The mechanism of proton transport by the UCPs is unresolved. UCPs may also transport fatty acids or fatty acyl peroxides. Several physiological functions of UCPs are postulated. (1) UCP1 is specialised for thermogenesis; UCP3 and avian UCPs possibly share this function. (2) UCPs may attenuate ROS production and protect against oxidative damage, degenerative diseases and ageing. (3) UCP3 may catalyse fatty acid transport. (4) UCP2 has a signalling role in pancreatic β cells, where it attenuates insulin secretion. Other roles remain to be discovered.